Nasal tolerance in experimental autoimmune myasthenia gravis (EAMG): induction of protective tolerance in primed animals. 1998

F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
Division of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.

Nasal administration of microg doses of acetylcholine receptor (AChR) is effective in preventing the development of B cell-mediated EAMG in the Lewis rat, a model for human MG. In order to investigate whether nasal administration of AChR modulates ongoing EAMG, Lewis rats were treated nasally with AChR 2 weeks after immunization with AChR and Freund's complete adjuvant. Ten-fold higher amounts of AChR given nasally (600 microg/rat) were required to ameliorate the manifestations of EAMG compared with the amounts necessary for prevention of EAMG. In lymph node cells from rats receiving 600 microg/rat of AChR, AChR-induced proliferation and interferon-gamma (IFN-gamma) secretion were reduced compared with control EAMG rats receiving PBS only. The anti-AChR antibodies in rats treated nasally with 600 microg/rat of AChR had lower affinity, reduced proportion of IgG2b and reduced capacity to induce AChR degradation. Numbers of AChR-reactive IFN-gamma and tumour necrosis factor-alpha (TNF-alpha) mRNA-expressing lymph node cells from rats treated nasally with 600 microg/rat of AChR were suppressed, while IL-4, IL-10 and transforming growth factor-beta (TGF-beta) mRNA-expressing cells were not affected. Collectively, these data indicate that nasal administration of AChR in ongoing EAMG induced selective suppression of Th1 functions, i.e. IFN-gamma and IgG2b production, but no influence on Th2 cell functions. The impaired Th1 functions may result in the production of less myasthenic anti-AChR antibodies and contribute to the amelioration of EAMG severity in rats treated with AChR 600 microg/rat by the nasal route.

UI MeSH Term Description Entries
D007074 Immunoglobulin G The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B. Gamma Globulin, 7S,IgG,IgG Antibody,Allerglobuline,IgG(T),IgG1,IgG2,IgG2A,IgG2B,IgG3,IgG4,Immunoglobulin GT,Polyglobin,7S Gamma Globulin,Antibody, IgG,GT, Immunoglobulin
D007108 Immune Tolerance The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc. Immunosuppression (Physiology),Immunosuppressions (Physiology),Tolerance, Immune
D007132 Immunoglobulin Isotypes The classes of immunoglobulins found in any species of animal. In man there are nine classes that migrate in five different groups in electrophoresis; they each consist of two light and two heavy protein chains, and each group has distinguishing structural and functional properties. Antibody Class,Ig Isotype,Ig Isotypes,Immunoglobulin Class,Immunoglobulin Isotype,Antibody Classes,Immunoglobulin Classes,Class, Antibody,Class, Immunoglobulin,Classes, Antibody,Classes, Immunoglobulin,Isotype, Ig,Isotype, Immunoglobulin,Isotypes, Ig,Isotypes, Immunoglobulin
D008213 Lymphocyte Activation Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION. Blast Transformation,Blastogenesis,Lymphoblast Transformation,Lymphocyte Stimulation,Lymphocyte Transformation,Transformation, Blast,Transformation, Lymphoblast,Transformation, Lymphocyte,Activation, Lymphocyte,Stimulation, Lymphocyte
D009157 Myasthenia Gravis A disorder of neuromuscular transmission characterized by fatigable weakness of cranial and skeletal muscles with elevated titers of ACETYLCHOLINE RECEPTORS or muscle-specific receptor tyrosine kinase (MuSK) autoantibodies. Clinical manifestations may include ocular muscle weakness (fluctuating, asymmetric, external ophthalmoplegia; diplopia; ptosis; and weakness of eye closure) and extraocular fatigable weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles (ocular myasthenia). THYMOMA is commonly associated with this condition. Anti-MuSK Myasthenia Gravis,MuSK MG,MuSK Myasthenia Gravis,Muscle-Specific Receptor Tyrosine Kinase Myasthenia Gravis,Muscle-Specific Tyrosine Kinase Antibody Positive Myasthenia Gravis,Myasthenia Gravis, Generalized,Myasthenia Gravis, Ocular,Anti MuSK Myasthenia Gravis,Generalized Myasthenia Gravis,Muscle Specific Receptor Tyrosine Kinase Myasthenia Gravis,Muscle Specific Tyrosine Kinase Antibody Positive Myasthenia Gravis,Myasthenia Gravis, Anti-MuSK,Myasthenia Gravis, MuSK,Ocular Myasthenia Gravis
D011917 Rats, Inbred Lew An inbred strain of rat that is used in BIOMEDICAL RESEARCH. Rats, Inbred Lewis,Rats, Lew,Inbred Lew Rat,Inbred Lew Rats,Inbred Lewis Rats,Lew Rat,Lew Rat, Inbred,Lew Rats,Lew Rats, Inbred,Lewis Rats, Inbred,Rat, Inbred Lew,Rat, Lew
D011950 Receptors, Cholinergic Cell surface proteins that bind acetylcholine with high affinity and trigger intracellular changes influencing the behavior of cells. Cholinergic receptors are divided into two major classes, muscarinic and nicotinic, based originally on their affinity for nicotine and muscarine. Each group is further subdivided based on pharmacology, location, mode of action, and/or molecular biology. ACh Receptor,Acetylcholine Receptor,Acetylcholine Receptors,Cholinergic Receptor,Cholinergic Receptors,Cholinoceptive Sites,Cholinoceptor,Cholinoceptors,Receptors, Acetylcholine,ACh Receptors,Receptors, ACh,Receptor, ACh,Receptor, Acetylcholine,Receptor, Cholinergic,Sites, Cholinoceptive
D004195 Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases. Animal Disease Model,Animal Disease Models,Disease Model, Animal
D005260 Female Females
D005620 Freund's Adjuvant An antigen solution emulsified in mineral oil. The complete form is made up of killed, dried mycobacteria, usually M. tuberculosis, suspended in the oil phase. It is effective in stimulating cell-mediated immunity (IMMUNITY, CELLULAR) and potentiates the production of certain IMMUNOGLOBULINS in some animals. The incomplete form does not contain mycobacteria. Freund Adjuvant,Adjuvant, Freund,Adjuvant, Freund's,Freunds Adjuvant

Related Publications

F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
November 2014, Journal of autoimmunity,
F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
May 1985, Acta pathologica japonica,
F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
August 1997, Clinical and experimental immunology,
F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
May 1998, Journal of neuroimmunology,
F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
October 2000, Journal of immunology (Baltimore, Md. : 1950),
F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
January 2005, Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban,
F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
January 1993, International journal of immunopharmacology,
F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
February 1997, Journal of autoimmunity,
F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
January 1997, Clinical and experimental immunology,
F D Shi, and X F Bai, and H L Li, and Y M Huang, and P H Van der Meide, and H Link
January 1988, Monographs in allergy,
Copied contents to your clipboard!